Endoplasmic Reticulum Stress and Pathogenesis of Vascular Calcification

Frontiers in Cardiovascular Medicine

Yidan Zheng¹  Zhejun Cai²  Zhenqi Rao³  Li Xu³  Fei Li³  Nianguo Dong³  Zihao Wang³  Ming Chen³  Ying Zhou³ 

[1] Basic Medical School, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;Department of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China;Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China;

关键词: vascular calcification;    endoplasmic reticulum stress;    unfolded protein response;    chronic kidney disease;    atherosclerosis;    diabetes;   

DOI  :  10.3389/fcvm.2022.918056

来源: DOAJ

【 摘 要 】

Vascular calcification (VC) is characterized by calcium phosphate deposition in blood vessel walls and is associated with many diseases, as well as increased cardiovascular morbidity and mortality. However, the molecular mechanisms underlying of VC development and pathogenesis are not fully understood, thus impeding the design of molecular-targeted therapy for VC. Recently, several studies have shown that endoplasmic reticulum (ER) stress can exacerbate VC. The ER is an intracellular membranous organelle involved in the synthesis, folding, maturation, and post-translational modification of secretory and transmembrane proteins. ER stress (ERS) occurs when unfolded/misfolded proteins accumulate after a disturbance in the ER environment. Therefore, downregulation of pathological ERS may attenuate VC. This review summarizes the relationship between ERS and VC, focusing on how ERS regulates the development of VC by promoting osteogenic transformation, inflammation, autophagy, and apoptosis, with particular interest in the molecular mechanisms occurring in various vascular cells. We also discuss, the therapeutic effects of ERS inhibition on the progress of diseases associated with VC are detailed.

【 授权许可】

Unknown